Das U, Wang L, Ganguly A, Saikia JM, Wagner SL, Koo EH, Roy S (2016). Visualizing APP and BACE-1 approximation in neurons yields insight into the amyloidogenic pathway. Nat Neurosci. 2015 Dec 7 issue
Ganguly A, Tang Y, Wang L, Ladt K, Loi J, Dargent D, Leterrier C, and Roy S (2015). A dynamic formin-dependent deep F-actin network in axons. Journal of Cell Biology, July 27 issue; 210(3).
Wang L, Das U, Scott D, Tang Y, McLean P and Roy S (2014). Alpha-Synuclein Multimers Cluster Synaptic Vesicles and attenuate Recycling. Current Biology, 2014 Sep 24. (14)01040-9.
Tang Y, Scott D, Das U, Gitler D, Ganguly S, and Roy S (2013). Fast vesicle transport is required for the slow axonal transport of synapsin.
Journal of Neuroscience, 33(39):15362-15375.
Das U, Scott D, Koo EH, Tang Y and Roy S. (2013) Activity-induced convergence of APP and BACE-1 in acidic microdomains via an endocytosis-dependent pathway.
Neuron, Aug. 7 issue.
Scott D and Roy S. (2012) Alpha-synuclein inhibits inter-synaptic vesicle mobility and maintains recycling pool homeostasis.
Journal of Neuroscience, July 25; 32(30):10129-35.
Roy S, Yang Ge, Tang Y and Scott D. (2011). A simple photo-activation and image-analysis module for visualizing and analyzing axonal transport with high temporal resolution.
Nature Protocols; 7:62-8.
Scott D, Das U, Tang Y and Roy S. (2011) Mechanistic logic underlying the axonal transport of cytosolic proteins.
Scott D, Tabarean I, Tang Y, Cartier A, Masliah E, Roy S. (2010) A pathologic cascade leading to synaptic dysfunction in α-synuclein-induced neuro-degeneration
Journal of Neuroscience 16;30(24):8083-95.
Tang Y, Scott D, Das U, Edland S, Radomski K, Koo E and Roy
S. (2012) Early and selective impairments in axonal transport kinetics of synaptic cargoes induced by soluble amyloid-beta protein oligomers.
"The science of living things is the science of movement and transformation" - attributed to Leonardo DaVinci.
Cell Biology of neuronal trafficking in physiology and neurodegenerative diseases:
Due to their complex geometry and finite sites of bulk protein synthesis (perikarya), neurons have evolved elaborate transport and trafficking machineries to deliver proteins into axons and dendrites. How are somatically-synthesized proteins delivered to their appropriate sites, and then retained there (for example at the synaptic terminals)? Knowledge into the biology of this process is critical for determining neuronal form and function; and also to understand how these processes go awry in disease.
A general approach in the lab is to develop accurate cellular models of normal and abnormal biological phenotypes – using dissociated neurons from mice, drosophila neurons in-vivo, 3-D organoids, and induced pluripotent stem cells (iPSC's; see http://www.roylab.org/publications.html for list of publications). Current projects include novel uses of CRISPR-Cas9 technology in cellular model-systems of neurodegenerative diseases – particularly Alzheimer’s disease; development and application of new tools (including super-resolution microscopy and optogenetics) to explore axonal transport and intricacies of the neuronal cytoskeleton (particularly actin); and use of iPSC’s to explore human cell biology. A guiding philosophy in the lab is to use whatever tools are needed to explore the question at hand, and whenever necessary, build new ones.
The lab has ongoing collaborations with researchers at the Wisconsin Institute for Discovery (WID), the Waisman Center, the Wisconsin Alzheimer’s Center, as well as several other investigators at UW-Madison; and is located on state of the art laboratory and office space overlooking lake Mendota (within the Wisconsin Institute for Medical Research or WIMR-II tower: WIMR-II-science-without-walls).